Alterations in "vascular reactivity" have often been invoked to explain the increase in peripheral resistance that is attendant with all forms of hypertension. The microcirculatory elements most responsible for this increase in resistance are the arterioles, yet few studies have primarily concerned themselves with factors that can directly affect arteriolar responsiveness in vivo. Most investigations involve the study of large blood vessels either in vitro or in vivo. The basic mechanism(s) leading to increased vasoconstrictor responsiveness of small blood vessels in various forms of hypertension is at the present time unknown. The proposed research seeks to implicate the involvement of prostaglandins (PGs) in the genesis of hypertension. The experimental approach includes the visualization and quantification of microvasuclar changes in spontaneously hypertensive and control rats in vivo, in response to exogenously applied or endogenously released arachidonic acid (AA) and the biochemical products of the arachidonic acid enzymatic cascade (PGs, endoperoxides and thromboxane). Normotensive and hypertensive animals will be compared to determine if sensitivity or intrinsic activity of arterioles is altered to these substances. Various physiologic and pharmacologic manipulations will be performed to assess the ability of hypertensive animals to mobilize endogenous stores of AA for the production of vasodilator PGs; additionally, precursors of PGs, i.e., AA and endoperoxides will be administered in order to reveal any difference in utilization and product formation. With this approach three essential questions concerning the role of prostaglandins in hypertension could be answered. 1. Is there an attenuated responsiveness to vasodilator PGs in hypertension? 2. Are hypertensive animals unable to mobilize in physiologic circumstances or during hormonal stimulation prostaglandin precursors and hence, are unable to buffer vasoconstrictor-vasopressor stimuli? And 3. Do Hypertensive animals utilize PG precursors differently from normal animals and how this might contribute to the hypertensive state?